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reality shifting in latency
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sorry too lazy rn for citations
Melatonin is a signalling molecule to promote stress resistance, a zeitgeber, and probably a youth signal. Levels peak in early childhood (1-3 years approx) after circadian processes develop. The decline in levels in childhood has been proposed to be mediated by the increase in body size, thus diluting the melatonin. A further decline is associated with the onset of puberty, and there is evidence showing that exogenous melatonin can delay puberty – would it be reasonable to frame this as melatonin signalling to the body that the organism is younger than it is and thus delay puberty? Clinical trials of melatonin in older adults have shown positive results in ameliorating health conditions. Curiously, the pineal gland is prone to becoming calcified (presumably detrimental to hormonal production) even as early as school-age. Melatonin is synthesized from N-acetyl serotonin catalyzed by acetylserotonin O-methyltransferase in some but not all prokaryotes and eukaryotes. Melatonin is used as a signalling molecule to promote protection from environmental stressors, and the metabolites of melatonin such as N(1)-acetyl-N(2)-formyl-5-methoxykynuramine (AFMK) also have been show to play a cascade of related roles. In many animals, the pineal gland is the main producer of hormonal melatonin, and its origin is probably related to the parietal eye, a third eye found on the head of tuataras where it is considered vestigial. The stimulus for the pineal gland to produce hormonal melatonin is absense of light in the retina. In ancient evolution, melatonin probably was used up during the day to protect from the harsh sunlight and therefore a circadian rhythm was established based on the phenomenon of elevated melatonin at night. Melatonin also has paracrine function and can be produced in the skin and eyes in response to sunlight. The mitochondria also can produce melatonin. Oral melatonin supplements have a bioavailibility of approx 15% but may vary, and oral melatonin has been shown to interact with the gut microbiome. It is not completely understood how exogenous melatonin impacts endogenous production and sensitivity across tissues and organisms but appears safe with no long-term harm. Oral melatonin has a short serum half life, estimated between 20 minutes and 2 hours. It must be noted that the circadian effect on the central nervous system requires serum melatonin to transfer into the cerbrospinal fluid system, and therefore a higher-than-physiological serum level is probably required for full effect. The half-life in the CSF system is probably longer due to lower metabolism of melatonin. Oral melatonin can promote sleep onset, potentially by acting as a zeitgeber or by promoting GABAergic signalling. Melatonin has also been shown to increase REM sleep, GH levels, osteoblast activity, and promote a natural decrease of body temperature and insulin associated with sleep. Being a signalling molecule, melatonin affects gene expression in myriad ways, with two receptors named after it (MT1 & MT2). Melatonin receptors may be desensitized by high levels of melatonin, but their sensitivity appears to fluctuate on a daily basis. Melatonin has been shown to extend maximum lifespan in flies and some but not all cases in mice, and at least one study showed dramatic reduction of markers of DNA damage in mice dependent on the duration melatonin was given over their lifetime at a dose of 2 mg/L. Notably, melatonin acts to promote wakefulness in nocturnal animals such as mice.
Melatonin is a signalling molecule to promote stress resistance, a zeitgeber, and probably a youth signal. Levels peak in early childhood (1-3 years approx) after circadian processes develop. The decline in levels in childhood has been proposed to be mediated by the increase in body size, thus diluting the melatonin. A further decline is associated with the onset of puberty, and there is evidence showing that exogenous melatonin can delay puberty – would it be reasonable to frame this as melatonin signalling to the body that the organism is younger than it is and thus delay puberty? Clinical trials of melatonin in older adults have shown positive results in ameliorating health conditions. Curiously, the pineal gland is prone to becoming calcified (presumably detrimental to hormonal production) even as early as school-age. Melatonin is synthesized from N-acetyl serotonin catalyzed by acetylserotonin O-methyltransferase in some but not all prokaryotes and eukaryotes. Melatonin is used as a signalling molecule to promote protection from environmental stressors, and the metabolites of melatonin such as N(1)-acetyl-N(2)-formyl-5-methoxykynuramine (AFMK) also have been show to play a cascade of related roles. In many animals, the pineal gland is the main producer of hormonal melatonin, and its origin is probably related to the parietal eye, a third eye found on the head of tuataras where it is considered vestigial. The stimulus for the pineal gland to produce hormonal melatonin is absense of light in the retina. In ancient evolution, melatonin probably was used up during the day to protect from the harsh sunlight and therefore a circadian rhythm was established based on the phenomenon of elevated melatonin at night. Melatonin also has paracrine function and can be produced in the skin and eyes in response to sunlight. The mitochondria also can produce melatonin. Oral melatonin supplements have a bioavailibility of approx 15% but may vary, and oral melatonin has been shown to interact with the gut microbiome. It is not completely understood how exogenous melatonin impacts endogenous production and sensitivity across tissues and organisms but appears safe with no long-term harm. Oral melatonin has a short serum half life, estimated between 20 minutes and 2 hours. It must be noted that the circadian effect on the central nervous system requires serum melatonin to transfer into the cerbrospinal fluid system, and therefore a higher-than-physiological serum level is probably required for full effect. The half-life in the CSF system is probably longer due to lower metabolism of melatonin. Oral melatonin can promote sleep onset, potentially by acting as a zeitgeber or by promoting GABAergic signalling. Melatonin has also been shown to increase REM sleep, GH levels, osteoblast activity, and promote a natural decrease of body temperature and insulin associated with sleep. Being a signalling molecule, melatonin affects gene expression in myriad ways, with two receptors named after it (MT1 & MT2). Melatonin receptors may be desensitized by high levels of melatonin, but their sensitivity appears to fluctuate on a daily basis. Melatonin has been shown to extend maximum lifespan in flies and some but not all cases in mice, and at least one study showed dramatic reduction of markers of DNA damage in mice dependent on the duration melatonin was given over their lifetime at a dose of 2 mg/L. Notably, melatonin acts to promote wakefulness in nocturnal animals such as mice.
